Tony Goldstone attended medical school at both Cambridge and Oxford Universities, and trained in general medicine, adult endocrinology and diabetes at the Hammersmith, St. Bartholomew’s and Royal London Hospitals in London. He obtained his Ph.D. from Imperial College London on the hypothalamic control of feeding and metabolism.
He has researched and published widely on hormonal control of appetite, neuroendocrine, hypothalamic and metabolic abnormalities in obesity and the genetic Prader-Willi syndrome, particularly investigating the causes of hyperphagia, through pre-clinical, clinical, post-mortem, genetic, interventional, fat and brain imaging studies. This includes work as a research fellow at the Netherlands Institute for Brain Research in Amsterdam and the Division of Pediatric Genetics at the University of Florida, USA.
He was a Senior Clinician Scientist in the Metabolic and Molecular Imaging Group, MRC Clinical Sciences Centre, Imperial College London until 2014, and is now based in the Computational, Cognitive and Clinical Neuroimaging Laboratory in the Division of Brain Sciences, at Hammersmith Hospital. A major theme of his current work is using functional MRI and body fat MRI to investigate appetite, eating behaviour and obesity, and the links with addictive behaviours, as well as the pathophysiology of genetic obesity, and hormonal and metabolic influences on and consequences of traumatic brain injury.
He has been a Consultant Endocrinologist at Imperial College Healthcare NHS Trust since 2005 based at the Hammersmith Hospital and St. Mary's Hospital. He runs specialist adult and paediatric clinics for patients with Prader-Willi syndrome and genetic obesity, and endocrine dysfunction after traumatic brain injury (in a multi-disciplinary clinic with Neurology and Psychiatry), as well as in-patient work within Endocrinology, Diabetes and Acute Medicine.
His public engagement work includes talks such as ‘Guts or Brain? Where hormones regulate appetite’, Food, Glorious Food! British Neuroscience Association Christmas Symposium 2011 at The Royal Society, London; ‘Obesity: what lies in weight?’, Edinburgh Science Festival 2013; ‘Separating the Fat from the Fiction: Food choices’, Edinburgh Science Festival 2014. His research has featured in several TV programs including BBC1 ‘10 Things You Need to Know about Losing Weight’, Channel 4 ‘Embarrassing Fat Bodies’, BBC Horizon ‘The Truth about Fat’, BBC2 ‘The Men Who Made us Fat’, and BBC Scotland ‘Addicted to Pleasure’, and in the BBC Science video ‘What is fat?’.
et al., 2016, Increased colonic propionate reduces anticipatory reward responses in the human striatum to high-energy foods., Am J Clin Nutr, Vol:104, Pages:5-14
et al., 2016, Prevalence and Correlates of Vitamin D Deficiency in Adults after Traumatic Brain Injury., Clin Endocrinol (oxf)
et al., 2016, Link Between Increased Satiety Gut Hormones and Reduced Food Reward After Gastric Bypass Surgery for Obesity, Journal of Clinical Endocrinology & Metabolism, Vol:101, ISSN:0021-972X, Pages:599-609
et al., 2014, Obese patients after gastric bypass surgery have lower brain-hedonic responses to food than after gastric banding, Gut, Vol:63, ISSN:0017-5749, Pages:891-902
et al., 2014, Ghrelin mimics fasting to enhance human hedonic, orbitofrontal cortex, and hippocampal responses to food, American Journal of Clinical Nutrition, Vol:99, ISSN:0002-9165, Pages:1319-1330
et al., 2014, Hyperphagia: Current Concepts and Future Directions Proceedings of the 2nd International Conference on Hyperphagia, Obesity, Vol:22, ISSN:1930-7381, Pages:S1-S17
et al., 2013, Pituitary Dysfunction after Blast Traumatic Brain Injury: The UK BIOSAP Study, Annals of Neurology, Vol:74, ISSN:0364-5134, Pages:527-536
et al., 2013, Loss-of-function mutations in SIM1 contribute to obesity and Prader-Willi-like features, Journal of Clinical Investigation, Vol:123, ISSN:0021-9738, Pages:3037-3041
et al., 2012, Gastric bypass surgery for obesity decreases the reward value of a sweet-fat stimulus as assessed in a progressive ratio task, American Journal of Clinical Nutrition, Vol:96, ISSN:0002-9165, Pages:467-473
et al., 2012, The Missing Risk: MRI and MRS Phenotyping of Abdominal Adiposity and Ectopic Fat, Obesity, Vol:20, ISSN:1930-7381, Pages:76-87
et al., 2009, Fasting biases brain reward systems towards high-calorie foods, European Journal of Neuroscience, Vol:30, ISSN:0953-816X, Pages:1625-1635
et al., 2008, Recommendations for the Diagnosis and Management of Prader-Willi Syndrome, Journal of Clinical Endocrinology & Metabolism, Vol:93, ISSN:0021-972X, Pages:4183-4197
Goldstone AP, Beales PL, 2008, Genetic obesity syndromes, Frontiers of Hormone Research, Vol:36, ISSN:0301-3073, Pages:37-60
et al., 2005, Fasting and postprandial hyperghrelinemia in Prader-Willi syndrome is partially explained by hypoinsulinemia, and is not due to peptide YY3-36 deficiency or seen in hypothalamic obesity due to craniopharyngioma, Journal of Clinical Endocrinology & Metabolism, Vol:90, ISSN:0021-972X, Pages:2681-2690
et al., 2004, Somatostatin infusion lowers plasma ghrelin withoug reducing appetite in adults with Pradi-Willi syndrome, Journal of Clinical Endocrinology & Metabolism, Vol:89, ISSN:0021-972X, Pages:4162-4165
Goldstone AP, 2004, Prader-Willi syndrome: advances in genetics, pathophysiology and treatment, Trends in Endocrinology and Metabolism, Vol:15, ISSN:1043-2760, Pages:12-20
Goldstone AP, Unmehopa UA, Swaab DF, 2003, Hypothalamic growth hormone-releasing hormone (GHRH) cell number is increased in human illness, but is not reduced in Prader-Willi syndrome or obesity, Clinical Endocrinology, Vol:58, ISSN:0300-0664, Pages:743-755
et al., 2001, Visceral adipose tissue and metabolic complications of obesity are reduced in Prader-Willi syndrome female adults: Evidence for novel influences on body fat distribution, Journal of Clinical Endocrinology & Metabolism, Vol:86, ISSN:0021-972X, Pages:4330-4338